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OS3 Exam II > Cardiac Patient > Flashcards

Cardiac Patient Flashcards

1
Q

Treatment of the CV patient requires multiple avenues of treatment:

A
  • diet
  • medication
  • exercise
  • stress reduction
  • smoking cessation
  • integrate your treatment
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2
Q

Cardiac Sympathetics

A
  • origins in T1-6 with synapses in the upper thoracic and cervical chain ganglia
  • fibers originating from the right pass to the right deep cardiac plexus
  • fibers originating from the left pass through the left deep plexus and inverted AV node
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3
Q

Right deep cardiac plexus

A
  • innervates the SA node

- hyperactivity predisposes to supraventricular tachyarrhythmias

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4
Q

Left deep cardiac plexus

A
  • innervates AV node

- hyperstimulation predisposes to ectopic foci and ventricullar fibrillation

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5
Q

Increased sympathetic tone linked to

A
  • coronary vasospasm

- associated with increased morbidity post-MI (inhibits collateral circulation development)

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6
Q

Vessels are rich in sympathetics:

A
  • vasoconstriction: increases peripheral vascular resistance; produces a shunt from one area to another
  • decreased tone=vasodilation
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7
Q

Cardiac Parasympathetics

A
  • right vagus nerve primarily to SA node
  • left vagus nerve supplies AV node
  • visceral-visceral reflexes
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8
Q

Right vagus nerve hyperactivity

A

-leads to sinus bradyarrythmias

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9
Q

Left vagus nerve hyperactivity

A

leads to AV block

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10
Q

Visceral-visceral reflexes

A

-pulmonary branches strongest inhibitor reflex–aspiration

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11
Q

Visceral-visceral reflexes (slowing of heart rate)

A
  • irritation of larynx
  • pressure on carotid body
  • pressure on globe of eye (oculocardiac reflex): less affect in sympathecotonic patients; more affective in vagotonia patients
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12
Q

Vagal connections abundant at

A

OA, AA and C2 areas

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13
Q

PNS Vasculature involvement

A
  • submaxillary gland vessels
  • parotid gland vessels
  • vessels of blush region of face
  • vessels of tongue
  • vessels of the penis
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14
Q

Cardio Lymphatics

A
  • drainage from the heart and lungs mainly via the right lymphatic duct
  • impaired drainage known to severely compromise homeostatic mechanisms: increased morbidity and mortality with ischemia and infection
  • peripherally, lymphatic congestion has been linked to atherosclerosis and HTN
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15
Q

Lymphatics play significant role in

A
  • pulmonary edema
  • ascites
  • hepatomegaly
  • peripheral edema in CHF: electrolyte imbalance develops; increases morbidity
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16
Q

Thoracic duct

A
  • under sympathetic control

- hypersympathetic activity can reduce flow

17
Q

Somatic involvement in Cardiac disease

A
  • severe scoliosis (75 degrees thoracic curve) compromises cardiac function
  • compensatory musculoskeletal problems reflexly affect cardiac function
  • must treat postural stressor
  • longer lasting changes to compensatory changes with OMM
18
Q

Somatic involvement in cardiac disease: gait

A
  • in patients with decreased cardiac output, abnormal gait patterns increase cardiac workload up to 300%
  • optimizing the gait pattern will give back strength to fulfill activities of daily living
19
Q

Somatic involvement in cardiac disease: anterior chest wall syndrome

A
  • generic term for a variety of causes for substernal and/or chest pains
  • often misdiagnosed as cardiac dysfunction
  • somatic factors do co-exist with cardiac disease
  • reduction in cardiac symptoms after OMM cannot rule out the need for further work-up or therapeutics in a given patient
20
Q

Somatic causes of chest pain

A
  • cervical, thoracic, sternal, rib dysfunction
  • costochondritis (Tietze’s syndrome)
  • intercostal neuritis
  • myofascial trigger points–pec major and minor
  • rib fractures
21
Q

Classic cardiac and coronary pattern of pain referral

A
  • upper left chest radiating out and down the inner surface of the arm and up into the neck and jaw
  • palpatory changes found mostly at levels of T2-4 on the left
22
Q

Anterior wall infarctions have more changes in

A

T1-4

23
Q

Pain referral: posterior and inferior wall MI

A
  • increased bradyarrhythmias
  • palpatory changes at C2: rich in vagal connections
  • may have an autonomic rationale for these changes
24
Q

Hypertension is strongly associated with

A

bilateral trophic changes at T5-7, T8-T10, and T11-L2

  • study controlled for age, sex, and other comorbid condition
  • diabetes T10-11
25
Q

Myocardial infarction

A
  • first treatment goal is to decrease SNS activity in upper thoracics
  • reduce inappropriate reflexes
  • lower risk of ectopic foci and ventricular fibrillation
  • remove at least one factor that discourages collateral circulation
  • use indirect techniques: paraspinal inhibition (lower peripheral resistance)
26
Q

MI Vagal stimulation

A
  • C2 and cranial base
  • inferior wall infarction
  • treat these areas to help decrease bradyarrhythmias, hypotension, and decreased coronary flow to ischemic tissue
27
Q

MI: Sympathetics

A
  • SNS stimulation of T1-6
  • more activity at T2-3 on the left: anterior wall infarction
  • treat these areas to help decrease risk of supra ventricular and ventricular arrythmias
28
Q

Myocardial Infarction: Lymphatics

A
  • treat thoracic inlet indirectly
  • if post-resuscitation: indirect treatment to ribs and sternum
  • pectoral traction; diaphragm addressed through thoracolumbar fascia (indirect)
29
Q

Hypertension: Multifactorial etiology

A
  • genetic
  • habitual factors
  • neurogenic
  • humoral (hormonal)
  • vascular
30
Q

HTN functional elements implicated

A
  • vascular and cardiac hyper-reactivity to sympathetic stimuli in most patients with HTN
  • prolonged SNS stimulation to kidneys leads to water and sodium retention
  • As BP increases, homeostatic mechanisms of the baroreceptors reset to maintain higher arterial pressure
31
Q

HTN Treatment

A
  • aimed at supporting the homeostatic mechanisms
  • Address the kidney and adrenal areas–actively involved in body homeostasis
  • Treat the whole spine: sympathetic innervation involves the entire spinal column
  • involves respiratory/fluid, neurologic and energy model
32
Q

HTN Chapman’s points

A
  • posterior T11-12
  • treatment by rotatory stimulation
  • systolic BP drop 15 mmHg
  • diastolic BP drop 8 mmHg
  • aldosterone down in 36 hours
33
Q

Congestive Heart Failure

A
  • diagnosis not just a symptom
  • find the cause and address it
  • treatment emphasis on: lymphatics and autonomics
  • when lymphatic channels are full and obstructed fluids “third space”–peripheral edema
  • thoracic duct dilation may occur with leakage causing ascites
34
Q

CHF Treatment

A
  • increased venous and lymphatic return will help increase cardiac output (especially after MI)
  • treat the thoracolumbar diaphragm: optimize the lymphatic pump
  • treatment to thoracic cage also helps with pumping mechanism
  • lymphatic pump and eflleurage/petrassage
35
Q

Arrythmia Treatment

A
  • modify vagal tone–oculocardiac reflex; carotid sinus; valsalva; OA/AA/C2
  • reduce segmental facilitation in the upper thoracics–addresses sympathetics

OS3 Exam II (10 decks)

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